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Plaque Bacteria (plaque + bacteria)
Kinds of Plaque Bacteria Selected AbstractsPeriodontal infection profiles in type 1 diabetesJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 12 2006Evanthia Lalla Abstract Objectives: We investigated the levels of subgingival plaque bacteria and serum IgG responses in patients with type 1 diabetes and non-diabetic controls of comparable periodontal status. Material and Methods: Fifty type 1 diabetes patients (mean duration 20.3 years, range 6,41) were age-and gender-matched with 50 non-diabetic individuals with similar levels of periodontal disease. Full-mouth clinical periodontal status was recorded, and eight plaque samples/person were collected and analysed by checkerboard hybridization with respect to 12 species. Homologous serum IgG titres were assessed by checkerboard immunoblotting. In a sub-sample of pairs, serum cytokines and selected markers of cardiovascular risk were assessed using multiplex technology. Results: Among the investigated species, only levels of Eubacterium nodatum were found to be higher in diabetic patients, while none of the IgG titres differed between the groups, both before and after adjustments for microbial load. Patients with diabetes had significantly higher serum levels of soluble E-selectin (p=0.04), vascular cell adhesion molecule-1 (VCAM-1; p=0.0008), adiponectin (p=0.01) and lower levels of plasminogen activator inhibitor-1 (PAI-1; p=0.02). Conclusions: After controlling for the severity of periodontal disease, patients with type 1 diabetes and non-diabetic controls showed comparable subgingival infection patterns and serum antibody responses. [source] Evaluation of the relationship between smoking during pregnancy and subgingival microbiotaJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2005Nurcan Buduneli Abstract Background: Numerous studies have shown that smoking negatively affects periodontal health. Hormonal changes, which occur during pregnancy have also been reported to have adverse effects on the periodontal tissues or indirectly through alterations in the subgingival bacterial flora. At present, no knowledge exists concerning possible effects of smoking on the composition of subgingival plaque in pregnancy. The purpose of the present study was to evaluate the effects of smoking during pregnancy on the subgingival plaque bacteria most commonly associated with periodontal disease. Methods: A total number of 181 women were examined within 72 h post-partum. Smoking status was recorded by means of a self-reported questionnaire and the study population was divided into three groups; non-smokers, light smokers, and heavy smokers. In each woman, two subgingival plaque samples were obtained from mesio- or disto-buccal aspect of randomly selected one molar and one incisor tooth by sterile paperpoints. Clinical periodontal recordings comprising presence of dental plaque, bleeding on probing (BOP), and probing pocket depth (PPD) were performed at six sites per each tooth at all teeth. Plaque samples were analysed by checkerboard DNA,DNA hybridization with respect to 12 bacterial species. In all analyses, the individual subject was the computational unit. Thus, mean values for all clinical parameters were calculated and bacterial scores from each individual sample were averaged. Statistical methods included ,2 test, Kruskal,Wallis test and Mann,Whitney U -test. Results: Mean ages were similar in the study groups. Plaque, BOP and PPD recordings were lower in the heavy-smoker group, but the differences were not statistically significant (p>0.05). The detection rates and bacterial loads of the specific subgingival bacteria exhibited no significant differences between the groups. No correlation could be found between smoking status and detection rates and bacterial loads of various bacterial species. Conclusion: The present findings suggest that smoking during pregnancy does not have a significant effect on the composition of subgingival plaque bacteria. [source] Recent concepts in plaque formationJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2003J.-P. Bernimoulin Abstract Dental plaque is an adherent, bacterial film, and is the main pathological agent for periodontal diseases. The formation of dental plaque can occur both supragingivally and subgingivally. The development of plaque is a three-step process. Following the formation of a pellicle, pioneer micro-organisms will adhere to it, proliferate and form colonies. The final stage involves the aggregation of filamentous organisms and spirochetes into a cohesive biofilm. Many products of the plaque bacteria reach the subepithelial tissue, causing inflammatory responses such as increased vascularity and leukocyte diapedesis. Both supragingival and subgingival plaque may form a hard, mineralized mass called calculus. The surface of calculus harbours bacteria, which may exacerbate the inflammatory responses. An effective oral antiseptic must be active against a wide range of Gram-positive and Gram-negative bacterial species, including streptococci and fusobacteria. Ideally, an effective agent would also penetrate the plaque biofilm. Data show that essential oil and chlorhexidine mouthwashes have the broadest antimicrobial effects. [source] Extracellular neutrophil traps in periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2009L. Vitkov Background and Objective:, Chronic periodontitis, the chronic inflammatory disease of the periodontium, is caused by bacteria and is characterized by an influx of neutrophils into the gingival crevice. Recently, a ,new' extracellular neutrophil defense mechanism , neutrophil extracellular traps , has been described. However, their role in periodontitis has not yet been investigated. Material and Methods:, Clinical examinations, transmission and scanning electron microscopy, as well as cytology and confocal laser-scanning microscopy, were employed to analyze gingiva biopsies and crevicular exudate from patients with chronic periodontitis. Results:, An abundance of neutrophil extracellular traps and some phagocytic neutrophils was found on the gingival pocket surface and in the purulent crevicular exudate. Finding neutrophil extracellular traps in the spontaneously effused purulent crevicular exudate clearly indicated that they are flushed from the pocket by the crevicular exudate. In cases of dispersal of subgingival plaque bacteria, their trapping by neutrophil extracellular traps in purulent crevicular exudate and on the gingival surface was demonstrated. Conclusion:, Trapping the crevicular bacteria prevents their adhesion to and invasion of the gingiva. The combination of neutrophil extracellular traps and crevicular exudate outflow appears to be a ,novel' defense mechanism for the clearance of crevicular bacteria in chronic periodontitis. [source] Upregulation of co-stimulatory molecule expression and dendritic cell marker (CD83) on B cells in periodontal diseaseJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2002Rangsini Mahanonda T cells and their cytokines are well known for their important role in the pathogenesis of periodontitis. To date, the role of antigen presenting cells (APCs), which are known to be critical in the regulation of T cell response, has been poorly investigated in periodontitis. In this study, we analyzed the expression of co-stimulatory molecules (CD80 and CD86) and CD83, which is a marker of mature dendritic cells, on gingival cells that were isolated from severe periodontitis tissues, with the use of flow cytometry. Significant upregulation of CD86 and CD83 expression was detected in periodontitis lesions, and most of this occurred on B cells. In vitro peripheral blood mononuclear cell cultures showed that stimulation with different periodontopathic bacteria, that included Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, and Actinomyces viscosus, upregulated both CD86 and CD83 expression on B cells. Therefore, the presence of plaque bacteria may be responsible for the enhanced expression seen in vivo on gingival B cells. APC function by bacterial-activated B cells was further investigated using allogeneic mixed leukocyte reactions. After 24 h culture with either A. actinomycetemcomitans or P. gingivalis, these activated B cells performed as potent APCs in mixed leukocyte reactions, and they stimulated T cells to produce high levels of gamma interferon and minimal interleukin-5. In conclusion, periodontopathic bacterial-induced B cell activation with upregulation of CD86 and CD83 may be associated with enhanced APC function. The results of this study suggest, therefore, that infiltrated gingival B cells have a possible role as APCs in the regulation and maintenance of local T cell response in periodontitis. [source] Cheese Consumption and the Development and Progression of Dental CariesNUTRITION REVIEWS, Issue 4 2002Shelby Kashket Ph.D. Whereas research into the causes of dental decay has focused on the harmful relationship between dental plaque bacteria and foods, studies into the protective effects of foods have been infrequent and limited in number. Recent investigations showed that milk and cheese could reduce the effects of metabolic acids, and could help restore the enamel that is lost during eating. Postulated mechanisms involve buffering, salivary stimulation, reduction of bacterial adhesion, reduction of enamel demineralization, and/or promotion of remineralization by casein and ionizable Ca and P. Given this information, consumers may be motivated to use milk and cheese to reduce, or reverse the cariogenic effects of many other foods. [source] Involvement of periodontopathic biofilm in vascular diseasesORAL DISEASES, Issue 1 2004K Okuda Oral bacteria inhabit biofilms, which are firm clusters adhering in layers to surfaces and are not easily eliminated by immune responses and are resistant to antimicrobial agents. Dental plaque is one such biofilm. In the past 10 years, subgingival plaque bacteria forming biofilms have been increasingly reported to be involved in systemic diseases. A close relationship between microbial infections and vascular disease has also been reported in the past two decades. The present review discusses the significance of the ecologic characteristics of biofilms formed by periodontopathic bacteria in order to further clarify the associations between periodontal disease and systemic disease. We focus on the relationships between periodontal disease-associated bacteria forming biofilms and vascular diseases including atherosclerosis and carotid coronary stenotic artery disease, and we discuss the direct and indirect effects on vascular diseases of lipopolysaccharides as well as heat shock proteins produced by periodontopathic bacteria. [source] |